rdf:type |
|
lifeskim:mentions |
umls-concept:C0001721,
umls-concept:C0003272,
umls-concept:C0024305,
umls-concept:C0332120,
umls-concept:C0383429,
umls-concept:C0393022,
umls-concept:C0439661,
umls-concept:C0596402,
umls-concept:C0599894,
umls-concept:C0683598,
umls-concept:C1555029,
umls-concept:C1709630,
umls-concept:C2733653
|
pubmed:issue |
12
|
pubmed:dateCreated |
2007-12-10
|
pubmed:abstractText |
In an attempt to define mechanisms by which B-cell non-Hodgkin lymphoma (NHL) may escape rituximab immunotherapy, we developed several rituximab-resistant cell lines (RRCL) generated from the rituximab-sensitive cell lines (RSCL) Raji and RL. Rituximab resistance was associated with CD20 downregulation and upregulation of CD52 and the complement inhibitory proteins (CIPs) CD55 and CD59. No significant alemtuzumab-associated complement-mediated cell lysis (CMC) or antibody-dependent cellular cytotoxicity (ADCC) was demonstrated in RSCL. In contrast, in vitro exposure of RRCL to alemtuzumab resulted in a significant degree of CMC and ADCC. Of note, in vitro blocking of CD52 with anti-CD52 F(ab')(2) fractions in RRCL improved rituximab-associated CMC as compared to unblocked RRCL. Our current data provides a basis for further evaluation of alemtuzumab-based clinical trials for patients with rituximab-resistant NHL.
|
pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal, Humanized,
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal...,
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD20,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/CD52 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Complement System Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/alemtuzumab,
http://linkedlifedata.com/resource/pubmed/chemical/rituximab
|
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
1042-8194
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
48
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
2424-36
|
pubmed:dateRevised |
2011-11-17
|
pubmed:meshHeading |
pubmed-meshheading:18067019-Antibodies, Monoclonal,
pubmed-meshheading:18067019-Antibodies, Monoclonal, Humanized,
pubmed-meshheading:18067019-Antibodies, Monoclonal, Murine-Derived,
pubmed-meshheading:18067019-Antibodies, Neoplasm,
pubmed-meshheading:18067019-Antibody-Dependent Cell Cytotoxicity,
pubmed-meshheading:18067019-Antigens, CD,
pubmed-meshheading:18067019-Antigens, CD20,
pubmed-meshheading:18067019-Antigens, Neoplasm,
pubmed-meshheading:18067019-Antineoplastic Agents,
pubmed-meshheading:18067019-Apoptosis,
pubmed-meshheading:18067019-Cell Line, Tumor,
pubmed-meshheading:18067019-Complement System Proteins,
pubmed-meshheading:18067019-Cytotoxicity, Immunologic,
pubmed-meshheading:18067019-Drug Resistance, Neoplasm,
pubmed-meshheading:18067019-Glycoproteins,
pubmed-meshheading:18067019-Histocompatibility Antigens Class II,
pubmed-meshheading:18067019-Humans,
pubmed-meshheading:18067019-Lymphoma, Non-Hodgkin
|
pubmed:year |
2007
|
pubmed:articleTitle |
CD52 over-expression affects rituximab-associated complement-mediated cytotoxicity but not antibody-dependent cellular cytotoxicity: preclinical evidence that targeting CD52 with alemtuzumab may reverse acquired resistance to rituximab in non-Hodgkin lymphoma.
|
pubmed:affiliation |
Department of Medicine, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
|